Tetrahydrobiopterin (BH4) is the rate-limiting cofactor for tyrosine hydroxylase (TH) and tryptophan hydroxylase, the initial enzymes which control thesynthetic rates of the catecholamines and serotonin. Prior neurochemical lesions in the nigrostriatal system of the rat with 6-hydroxydopamine (6-OHDA) indicated that the majority of BH4, TH, and GTP-cyclohydrolase (CH) are colocalized in striatal dopamine (DA) nerve terminals. Our studies using intrastriatal kainic acid (KA) injection indicated that 22 days after KA, TH, and BH4 were decreased by 25% and 30%, respectively. We now demonstrate that KA causes a 30% decrease in the protein to wet weight ratio (PWWR) in the lesioned striatum, which accounts for the observed changes in TH and BH4. Thus, results which express the concentration of striatal components after KA may vary depending on whether tissue protein or wet weight is used as the denominator. Our results demonstrate that KA doesn't cause significant DA terminal damage. Also, in Parkinson's disease, the site of decarboxylation of exogenously administered L-dopa doesn't occur in neurons whose cell bodies are located in the striatum. Rather, decarboxylation probably occurs in surviving DA and possibly serotonin terminals.